This document provides information about heparin-induced thrombocytopenia (HIT). It begins by introducing HIT as an immune-mediated reduction in platelet count that occurs in 3-5% of patients receiving unfractionated heparin for 5 days or more, and less than 1% for low molecular weight heparin. It then describes HIT as characterized by a platelet decrease of over 50% from baseline 5-10 days after starting heparin, along with hypercoagulability and heparin-dependent antibodies. The document outlines the pathogenesis of HIT and differences between type I and type II, reviews potential clinical complications, diagnostic methods, and emphasizes the need to promptly discontinue heparin and

1. HEPARIN INDUCED
THROMBOCYTOPENIA
(HIT)
Dr. Sayeedur Rahman Khan Rumi
Dr.rumibd@gmail.com
MD Cardiology Final Part Student
NHFH & RI

2. Introduction
• Heparin is a widely used anticoagulant drug for the treatment and
prevention of thromboembolic disorders
• Heparin may cause immune thrombocytopenia (a reduction in
platelet count), or HIT
• HIT occurs in approximately 3%-5% of patients during or after UFH
treatment for 5 days or more.
• The incidence is much lower, less than 1% during and after LMWH
therapy.
• HIT can cause life- or limb-threatening thromboses

3. Heparin Induced Thrombocytopenia
• Heparin induced thrombocytopenia (HIT) is characterized by a
decrease in the platelet count of more than 50% from the highest
platelet count value after the start of heparin, an onset 5 to 10 days
after the start of heparin, hypercoagulability, and the presence of
heparin dependent, platelet activating IgG antibodies.
• HIT is an immune-mediated potentially fatal syndrome in which the
heparin-induced immunoglobulins bridge platelets causing both
thrombocytopenia and thrombosis.
• HIT does not induce bleeding but rather results in a paradoxical
prothrombotic state.
• HIT is more common in surgical than medical patients (especially
cardiac and orthopaedic patients).

4. 1. Increased platelet destruction
• Non-immune
• Septicemia/Inflammation
• Disseminated intravascular coagulation
• Thrombotic thrombocytopenic purpura
• Immune
• Autoimmune: idiopathic or secondary immune thrombocytopenia
• Alloimmune: post-transfusion purpura
• Drug-induced: prothrombic (heparin), prohemorrhagic (quinine,
quinidine, gold, sulfa antibiotics, rifampin, vancomycin, NSAIDs, many
others)
Clinical Conditions/Causes of Thrombocytopenia

5. Clinical Conditions/Causes of Thrombocytopenia
(Cont‘d )
2. Decreased platelet production
• Alcohol, cytotoxic drugs
• Aplastic anemia
• Leukemia, myelodysplasia
• Metastatic invasion of marrow
• Certain infections
3. Hypersplenism
4. Hemodilution (infusion of blood products, colloids, or crystalloids)

6. TYPES OF HIT

7. Parameter Type I HIT
(non-immune mediated)
Type II HIT
(immune –mediated)
Epidemiology 10-30% of UFH treated patients 1-5% of UFH-treated patients
Less common with LMWH
Temporal pattern Between days 1-4 of initiating UFH Between days 4-16 of initiating
UFH/LMWH
Severity of
thrombocytopenia
Mild, usually platelet counts remain >
100,000
Moderate to severe, mean platelet count
60,000
Antibody-mediated No Yes
Thrombosis common No yes
Management Observe Discontinue heparin/LMWH and start
treatment with DTI
Outcome Self-limited Death, arterial and venous thromb-osis
are potential complications
Immune vs Non Immune-Mediated HIT

8. Pathogenesis of Heparin-Induced
Thrombocytopenia

9. Clinical events/Complications associated with HIT
Possible complications of HIT include the following:
• Deep venous thrombosis
• Pulmonary embolism
• Myocardial infarction
• Occlusion of limb arteries (possibly resulting in amputation)
• Transient ischemic attack and stroke
• Skin necrosis
• End-organ damage (eg, adrenal, bowel, spleen, gallbladder, or hepatic
infarction; renal failure)
• Death

10. Clinical signs of HIT
Erythematous plaques
Skin necrosis
Deep venous thrombosis
Venous gangrene

11. DIAGNOSIS OF HIT

13. Treatment of HIT
• The prompt cessation of heparin.
• As the condition is prothrombotic, these patients require alternative
anticoagulation (In the United States, lepirudin, argatroban, and
bivalirudin are licensed for HIT therapy)
• Prophylactic platelet transfusions should be avoided in patients with
HIT. The risk of bleeding is very low, and such transfusions can
increase the risk of thrombosis.
• The British Society of Haematology advises that all patients receiving
prolonged heparin of any sort should have platelet counts on day 1
and every 2-4 days.

14. Thank you